The immunopathology of Experimental Autoimmune Myasthenia Gravis (EAMG) in rats involves a neuromuscular impairment caused by a T cell-dependent antibody response produced against the post-junctional acetylcholine receptor (AChR). The result is weakness and rapid fatiguing in the rats similar to symptoms observed in human patients inflicted with myasthenia gravis. Although much information is known concerning the immunopathological role of AChR-reactive B cells (and the antibodies that they produce), much less is understood concerning the exact nature of AChR-reactive T cells. Furthermore, there is a paucity of information regarding effects of anti-AChR immune responses on neuromuscular signals resulting in muscle contraction. Thus, the goals of the proposed studies are to determine the influence of helper T cell specificity on subsequent anti-AChR antibody production and ultimately, the influence of helper T cell specificity on the induction of disease symptoms. A thorough understanding of the T cell regulation of this autoimmune antibody response may allow the development of immunotherapeutic strategies that augment or place currently in use.